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铅通过胶质细胞诱发神经毒性的研究进展

Research progress on Pb-induced neurotoxicity through glial cells
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摘要 铅是我国最主要的职业性有害因素之一,职业性铅中毒是铅中毒最主要的原因。铅可通过空气、食物、饮用水、皮肤等进入人体,在体内的多个器官蓄积,给人体造成健康风险,尤其是铅作业工人。既往许多研究表明铅可影响小胶质细胞、星形胶质细胞以及少突胶质细胞等胶质细胞的功能,产生不可逆转的神经损伤。本文概述铅通过胶质细胞诱导的神经毒性机制,阐述铅可诱导阿尔茨海默病、帕金森病和肌萎缩侧索硬化等神经退行性疾病,并对铅和胶质细胞的关系进行综述,为进一步研究铅对胶质细胞的神经毒性机制提供参考。 Lead is one of the most important occupational hazards in China,and occupational exposure is the leading cause of lead poisoning.Lead can be absorbed by the body through air,food,drinking water and skin,and accumulate in multiple organs in the body,posing health risks to humans,especially to lead workers.Many previous studies have shown that lead can affect the function of glial cells such as microglia,astrocytes and oligodendrocytes,resulting in irreversible neurological damage.This article provides an overview of the neurotoxic mechanism induced by lead through glial cells,elucidates that lead can induce neurodegenerative diseases such as Alzheimer′s disease,Parkinson′s disease,and amyotrophic lateral sclerosis,and reviews the relationship between lead and glial cells,in order to provide reference for further research on the neurotoxic mechanism of lead on glial cells.
作者 罗娜 王锦 张子阳 赵新元 黄荣荣 吴启运 Luo Na;Wang Jin;Zhang Ziyang;Zhao Xinyuan;Huang Rongrong;Wu Qiyun(Department of Occupational Medicine and Environmental Toxicology,School of Public Health,Nantong University,Nantong 226000,China;Nantong Key Laboratory of Environmental Toxicology,Nantong 226000,China;Department of Pharmacy,Affiliated Hospital of Nantong University,Nantong 226000,China)
出处 《中华预防医学杂志》 CAS CSCD 北大核心 2024年第10期1610-1615,共6页 Chinese Journal of Preventive Medicine
基金 国家自然科学基金(82173482,82173554,82101593)。
关键词 小胶质细胞 星形胶质细胞 少突胶质细胞 细胞活化 神经退行性疾病 Lead Microglia Astrocytes Oligodendrocytes Cell activation Neurodegenerative diseases
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  • 1孙黎光,邢伟,刘素媛,彭德才.神经系统铅中毒的分子机制[J].解剖科学进展,1995,1(2):177-182. 被引量:1
  • 2陈青,刘传勇.星形胶质细胞的活化机制及功能研究[J].泰山医学院学报,2006,27(1):69-71. 被引量:1
  • 3张敬军.星形胶质细胞的研究[J].中国药理学通报,2006,22(7):788-791. 被引量:34
  • 4Seo J, Lee B K, Jin S U. Lead-induced impairments in the neural processes related to working memory function [ J/OL ]. PLoS One, 2014, 9 (8): e105308, doi: 10. 1371/journal. pone. 0105308. eCollection 2014.
  • 5Neal A P, Guilarte T R. Mechanisms d lead and manganese neuroto:dcity [J]. Toxieal Res (Camb), 2013, 2(2): 99 -114.
  • 6Mortimer J A, Borenstein A R, Nelson L M. Associaliom of welding and rmnganese exposure with Parkinson disease: review and meta-analysis [J]. Neurology, 2012, 79(11): 1174-1180.
  • 7Roth J A. Correlation between the biochemical pathways altered by mutated parkinson-related genes and chronic exposure to manganese [ J]. Neurotoxicology, 2014, 44:314-325.
  • 8April P N, Tomas R G. Mechanisms of lead and rese neurotoxicity [J]. Toxicol Res(Camb), 2013, 2(2): 99-114.
  • 9Neal A P, Stansfield K H, Worley P F, et al. Lead exposure during synaptogenesis alters vesicular proteins and impairs vesicular release : potential role of NMDA receptor-dependent BDNF signaling [ J ]. Toxicol Sci, 2010, 116(1) : 249 -263.
  • 10Li N, Qiao M, Zhang P, et al. Tl~e effects of early life lead exposure on the expression of glycogen synthase kinase-313 and insulin-like growth factor 1 receptor in the hippocampus of mouse pups[J]. Biol Trace Elem Res, 2016, 169(1) : 114-120.

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